eMedicine Specialties > Infectious Diseases > Skin and Soft-Tissue Infections

Pinta

Natalie C Klein, MD, PhD, Associate Professor, Department of Medicine, Division of Infectious Diseases, SUNY School of Medicine at Stony Brook; Associate Director, Winthrop-University Hospital

Updated: Nov 4, 2009

Introduction

Background

Pinta is an endemic treponematosis caused by Treponema carateum. It is an ancient disease that was first described in the 16th century in Aztec and Carib Amerindians. In 1938, treponemes indistinguishable from those that cause yaws and syphilis were demonstrated in lesions of a Cuban patient. Pinta is characterized by chronic skin lesions that occur primarily in young adults.

Pathophysiology

Like other treponematoses, pinta is classified into an early and late stage. The early stage comprises the initial lesion and the secondary lesions, while the late stage comprises the latent phase and tertiary stage.

After an incubation period of approximately 2-3 weeks, the initial lesion appears on the skin. The primary lesion is a papule or erythematosquamous plaque usually found on exposed surfaces of the legs, dorsum of the foot, forearm, or hands. The lesion slowly enlarges and becomes pigmented and hyperkeratotic. It is often accompanied by regional lymphadenopathy.

Disseminated lesions, referred to as pintids, are similar to the primary lesion and may appear 3-9 months after infection. These secondary lesions vary in size and location and become pigmented with age.

Late or tertiary pinta is characterized by disfiguring pigmentary changes, hypochromia, achromic lesions, and hyperpigmented and atrophic lesions. The pigmentary changes often produce a mottled appearance of the skin. Lesions may appear red, white, blue, violet, and brown.

Frequency

United States

Pinta does not occur in the United States.

International

Pinta occurs in scattered foci in rural areas of Central and South America. In the 1950s, about 1 million cases of pinta were reported in Central and South America. In the 1980s, 20% seropositivity was found in remote rural areas of Panama. The current prevalence of pinta is unknown, but only a few hundred cases have been reported per year.

Mortality/Morbidity

• Pinta is the most benign of the endemic treponematoses. The skin is the only organ involved.
• No neurologic, bone, or cardiac manifestations occur. No congenital form exists.

Sex

Both sexes are affected with equal frequency.

Age

• Pinta affects children and adults of all ages.
• The peak age of incidence is 15-30 years.

Clinical

History

• The exact mode of transmission is unknown, but pinta is probably transmitted by direct skin or mucous membrane contact.
• The initial lesion is usually found on an exposed part of the body.
• Pinta causes no constitutional symptoms.

Physical

• The initial lesion is a papule that slowly enlarges to become a pruritic plaque (see Image 1).
  
  

  

  Erythematosquamous plaque of early pinta. Perine PL, Hopkins DR, Niemel PLA, et al. Handbook of Endemic Treponematoses: Yaws, Endemic Syphilis, and Pinta. Geneva, Switzerland: World Health Organization; 1984.

  
  
• The dorsum of the foot and legs are the most common sites of lesions (see Image 2).
  
  

  

  Violaceous psoriatic plaque of early pinta. Perine PL, Hopkins DR, Niemel PLA, et al. Handbook of Endemic Treponematoses: Yaws, Endemic Syphilis, and Pinta. Geneva, Switzerland: World Health Organization; 1984.

  
  
• The regional lymph nodes may enlarge.
• Lesions become pigmented with age and may change colors from copper to grey to slate blue (see Image 3).
  
  

  

  Late pigmented pinta (blue variety). Perine PL, Hopkins DR, Niemel PLA, et al. Handbook of Endemic Treponematoses: Yaws, Endemic Syphilis, and Pinta. Geneva, Switzerland: World Health Organization; 1984.

  
  
• Late lesions become achromic or hyperpigmented.

Causes

• T carateum is the causative agent and is considered to be a separate species from Treponema pallidum.
• T carateum can be grown only in primates, and less is known about this treponeme than any of the others.

Differential Diagnoses

Leprosy
Syphilis
Yaws

Other Problems to Be Considered

Discoid lupus
Eczema
Neurodermatitis
Pityriasis Alba
Psoriasis
Tinea corporis
Tinea versicolor
Vitiligo
Chloasma
Tinea nigra
Morphea
Lichen sclerosis

Workup

Laboratory Studies

• Pinta is most often a clinical diagnosis.
• The nontreponemal and treponemal serologic tests used in diagnosing venereal syphilis are used for serodiagnosis of pinta.
• Treponemes can be demonstrated by darkfield examination of exudates from early lesions.
• Nontreponemal test results (ie, rapid plasma reagent [RPR], Venereal Disease Research Laboratory [VDRL] test) are positive in all stages of pinta except very early lesions. Confirmatory treponemal test results (ie, T pallidum hemagglutination [TPHA], microhemagglutination T pallidum [MHA-TP], fluorescent treponemal antibody absorption [FTA-Abs]) are also positive but are not practical in remote areas.

Histologic Findings

Findings of pinta and yaws are similar, but pinta does not cause ulcer formation. In early lesions, mild acanthosis is present with migration of lymphoid cells into the epidermis. In the late stage, irregular acanthosis or epidermal atrophy occurs. Treponemes can be demonstrated in the epidermis in primary and secondary lesions using silver stain. They are absent in late achromic lesions.

Treatment

Medical Care

After penicillin therapy, lesions become noninfectious in 24 hours.

Surgical Care

Surgery has no role in pinta treatment.

Medication

The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity, and to prevent complications.

Antibiotics

Benzathine penicillin is the DOC but should not be administered to patients who are allergic to penicillin. Alternative therapies include tetracycline or erythromycin.

Penicillin G benzathine (Bicillin LA)

Interferes with cell wall synthesis during active multiplication, resulting in bactericidal activity against susceptible microorganisms. Should not be administered to patients who are allergic to penicillin.

Dosing

Adult

2.4 million U IM as single dose in 2 injection sites

Pediatric

50,000 U/kg IM as single dose; not to exceed 2.4 million U

Interactions

Probenecid can increase penicillin effectiveness by decreasing clearance; coadministration of penicillin with tetracyclines can decrease effectiveness of penicillin

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in impaired renal function

Tetracycline (Achromycin, Sumycin)

Alternative to benzathine penicillin for patients who are allergic to penicillin. Treats gram-positive and gram-negative organisms, as well as mycoplasmal, chlamydial, and rickettsial infections. Inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunit(s).

Dosing

Adult

500 mg PO qid for 15 d

Pediatric

<8 years: Not recommended
>8 years: 25-50 mg/kg/d (10-20 mg/lb) PO qid

Interactions

Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; can decrease effects of PO contraceptives, causing breakthrough bleeding and increased risk of pregnancy; tetracyclines can increase hypoprothrombinemic effects of anticoagulants

Contraindications

Documented hypersensitivity; severe hepatic dysfunction

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (ie, last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines

Erythromycin (Erythrocin, E-Mycin, EES)

Indicated for the treatment of infections in children who are allergic to penicillin or women who are pregnant. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes causing RNA-dependent protein synthesis to arrest. In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, one half of the total daily dose may be taken q12h. For more severe infections, double the dose.

Dosing

Adult

500 mg PO qid pc for 15 d

Pediatric

30-50 mg/kg/d (15-25 mg/lb/d) PO divided q6-8h pc; double dose for severe infection

Interactions

Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis

Contraindications

Documented hypersensitivity; hepatic impairment

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI adverse effects are common (administer doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occurs

Follow-up

Further Inpatient Care

• Lesions become noninfectious within 24 hours of treatment.
• Skin lesions heal slowly.
• After treatment, nontreponemal titers should decline and eventually revert to negative.

Prognosis

• The prognosis is good. The skin is the only organ affected. Primary and secondary lesions usually heal within 6-12 months. Pigmentary changes persist in late lesions.

Miscellaneous

Medicolegal Pitfalls

• Failure to diagnose

Multimedia

Media file 1: Erythematosquamous plaque of early pinta. Perine PL, Hopkins DR, Niemel PLA, et al. Handbook of Endemic Treponematoses: Yaws, Endemic Syphilis, and Pinta. Geneva, Switzerland: World Health Organization; 1984.

Media file 2: Violaceous psoriatic plaque of early pinta. Perine PL, Hopkins DR, Niemel PLA, et al. Handbook of Endemic Treponematoses: Yaws, Endemic Syphilis, and Pinta. Geneva, Switzerland: World Health Organization; 1984.

Media file 3: Late pigmented pinta (blue variety). Perine PL, Hopkins DR, Niemel PLA, et al. Handbook of Endemic Treponematoses: Yaws, Endemic Syphilis, and Pinta. Geneva, Switzerland: World Health Organization; 1984.

References

1. Antal GM, Lukehart SA, Meheus AZ. The endemic treponematoses. Microbes Infect. Jan 2002;4(1):83-94. [Medline].

2. Chulay JD. Treponema Species (Yaws, Pinta, Bejel). In: Mandell, Douglas, Bennett eds. Principles and Practice of Infectious Diseases. 5^th ed. Philadelphia, Pa: Churchill Livingstone; 2000:(2)2490-4.

3. Engelkens HJ, Niemel PL, van der Sluis JJ, Meheus A, Stolz E. Endemic treponematoses. Part II. Pinta and endemic syphilis. Int J Dermatol. Apr 1991;30(4):231-8. [Medline].

4. Engelkens HJ, Vuzevski VD, Stolz E. Nonvenereal treponematoses in tropical countries. Clin Dermatol. Mar-Apr 1999;17(2):143-52; discussion 105-6. [Medline].

5. Farnsworth N, Rosen T. Endemic treponematosis: review and update. Clin Dermatol. May-Jun 2006;24(3):181-90. [Medline].

6. Giuliani M, Latini A, Palamara G, Maini A, Di Carlo A. The clinical appearance of pinta mimics secondary syphilis: another trap of treponematosis?. Clin Infect Dis. May 15 2005;40(10):1548; author reply 1548-9. [Medline].

7. Hook III EW. Treponemal infections. In: Guerrant RL, Walker DH, Weller PF, eds. Tropical Infectious Diseases: Principles, Pathogens, and Practice. Philadelphia, Pa: Churchill Livingstone; 1999:527-34.

8. Lupi O, Madkan V, Tyring SK. Tropical dermatology: bacterial tropical diseases. J Am Acad Dermatol. Apr 2006;54(4):559-78; quiz 578-80. [Medline].

9. Morand JJ, Simon F, Garnotel E, Mahé A, Clity E, Morlain B. [Overview of endemic treponematoses]. Med Trop (Mars). Feb 2006;66(1):15-20. [Medline].

10. Parish JL. Treponemal infections in the pediatric population. Clin Dermatol. Nov-Dec 2000;18(6):687-700. [Medline].

11. Rothschild B. Pinta: specific disease or anomalous skin reaction?. Clin Infect Dis. Sep 15 2005;41(6):914. [Medline].

12. Woltsche-Kahr I, Schmidt B, Aberer W, Aberer E. Pinta in Austria (or Cuba?): import of an extinct disease?. Arch Dermatol. Jun 1999;135(6):685-8. [Medline].

Keywords

pinta, azul, carate, endemic treponematosis, mal de pinto, Treponema carateum, T carateum, skin lesions, treponemes, pintids

Contributor Information and Disclosures

Author

Natalie C Klein, MD, PhD, Associate Professor, Department of Medicine, Division of Infectious Diseases, SUNY School of Medicine at Stony Brook; Associate Director, Winthrop-University Hospital
Natalie C Klein, MD, PhD is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, and New York County Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Thomas Herchline, MD, Professor of Medicine, Wright State University Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio
Thomas Herchline, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Richard B Brown, MD, FACP, Chief, Division of Infectious Diseases, Baystate Medical Center; Professor, Department of Internal Medicine, Tufts University School of Medicine
Richard B Brown, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
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